Somatostatin, alpha-MSH and ACTH1-24, injected intraventricularly augment the turnover rate of acetylcholine in the hippocampus. Surgical transection of the fimbria, cingulum or the perforant pathway does not block the intraventricular effect of these peptides. The results suggest that the increase in hippocampal turnover rate of acetylcholine may be caused by an interaction of the peptides with hippocampal receptors. Substance P and beta-endorphin which decrease the turnover rate of acetylcholine when administered intraventricularly are still active when injected intraseptally suggesting that this action can be initiated by the activation of peptide receptors, located on the septum.